Calcium-dependent protein kinases (CPKs) function as calcium sensors and play important roles in plant immunity. Loss of function of the exocyst complex subunit EXO70B1 leads to autoimmunity caused by activation of TN2, a truncated Toll/interleukin-1 receptor-nucleotide binding sequence protein. Here we show, based on a screen for suppressors of , that-activated autoimmune responses require However, the CPK5 homologs CPK4, CPK6, and CPK11, which were previously reported to function redundantly with CPK5 in effector-triggered immunity, did not contribute to-associated phenotypes, indicating that CPK5 plays a unique role in plant immunity. Overexpressing results in TN2-dependent autoimmunity and enhanced disease resistance, reminiscent of the phenotypes. Ectopic expression of in the mutant led to constitutive CPK5 protein kinase activity, which was not detectable in mutants. Furthermore, TN2 interacts with the CPK5 N-terminal variable and kinase domains, stabilizing CPK5 kinase activity in vitro. This work uncovers a direct functional link between an atypical immune receptor and a crucial component of early immune signaling: increased immunity in depends on TN2 and CPK5 and, in a positive feedback loop, TN2 keeps CPK5 enzymatically active beyond the initiating stimulus.

Phytohormones play an important role in development and stress adaptations in plants, and several interacting hormonal pathways have been suggested to accomplish fine-tuning of stress responses at the expense of growth. This work describes the role played by the CALCIUM-DEPENDENT PROTEIN KINASE CPK28 in balancing phytohormone-mediated development in Arabidopsis thaliana, specifically during generative growth. cpk28 mutants exhibit growth reduction solely as adult plants, coinciding with altered balance of the phytohormones jasmonic acid (JA) and gibberellic acid (GA). JA-dependent gene expression and the levels of several JA metabolites were elevated in a growth phase-dependent manner in cpk28, and accumulation of JA metabolites was confined locally to the central rosette tissue. No elevated resistance toward herbivores or necrotrophic pathogens was detected for cpk28 plants, either on the whole-plant level or specifically within the tissue displaying elevated JA levels. Abolishment of JA biosynthesis or JA signaling led to a full reversion of the cpk28 growth phenotype, while modification of GA signaling did not. Our data identify CPK28 as a growth phase-dependent key negative regulator of distinct processes: While in seedlings, CPK28 regulates reactive oxygen species-mediated defense signaling; in adult plants, CPK28 confers developmental processes by the tissue-specific balance of JA and GA without affecting JA-mediated defense responses.

"Priming" in plant phytopathology describes a phenomenon where the "experience" of primary infection by microbial pathogens leads to enhanced and beneficial protection of the plant against secondary infection. The plant is able to establish an immune memory, a state of systemic acquired resistance (SAR), in which the information of "having been attacked" is integrated with the action of "being prepared to defend when it happens again." Accordingly, primed plants are often characterized by faster and stronger activation of immune reactions that ultimately result in a reduction of pathogen spread and growth. Prerequisites for SAR are (a) the initiation of immune signalling subsequent to pathogen recognition, (b) a rapid defence signal propagation from a primary infected local site to uninfected distal parts of the plant, and (c) a switch into an immune signal-dependent establishment and subsequent long-lasting maintenance of phytohormone salicylic acid-based systemic immunity. Here, we provide a summary on protein kinases that contribute to these three conceptual aspects of "priming" in plant phytopathology, complemented by data addressing the role of protein kinases crucial for immune signal initiation also for signal propagation and SAR.

Summary Systemic acquired resistance (SAR) prepares infected plants for faster and stronger defense activation upon subsequent attacks. SAR requires an information relay from primary infection to distal tissue and the initiation and maintenance of a self‐maintaining phytohormone salicylic acid (SA)‐defense loop. In spatial and temporal resolution, we show that calcium‐dependent protein kinase CPK5 contributes to immunity and SAR. In local basal resistance, CPK5 functions upstream of SA synthesis, perception, and signaling. In systemic tissue, CPK5 signaling leads to accumulation of SAR‐inducing metabolite N‐hydroxy‐L‐pipecolic acid (NHP) and SAR marker genes, including Systemic Acquired Resistance Deficient 1 (SARD1) Plants of increased CPK5, but not CPK6, signaling display an ‘enhanced SAR’ phenotype towards a secondary bacterial infection. In the sard1‐1 background, CPK5‐mediated basal resistance is still mounted, but NHP concentration is reduced and enhanced SAR is lost. The biochemical analysis estimated CPK5 half maximal kinase activity for calcium, K50 [Ca2+], to be c. 100 nM, close to the cytoplasmic resting level. This low threshold uniquely qualifies CPK5 to decode subtle changes in calcium, a prerequisite to signal relay and onset and maintenance of priming at later time points in distal tissue. Our data explain why CPK5 functions as a hub in basal and systemic plant immunity.